Although the magnitude of type-I IFN induction by RANKL or TNFα is small (low picomolar concentrations) when compared with other stimuli such as toll-like receptor (TLR) stimulation or viral infection, the endogenous autocrine type-I IFNs show significant feedback inhibitory effects on osteoclast differentiation (Binder et al., 2017; Takayanagi et al., 2002; Inoue et al., 2018). Here, TNFSF11 is linked to viral infectious disease.